alexa A Chimeric Protein (mTcd138) Comprising The Glucosyltransferase And Domains Of Toxin B And The Receptor Binding Domain Of Toxin A Provides Full Protection Against Clostridium Difficile Infection In Mice
ISSN: 2155-9597

Journal of Bacteriology & Parasitology
Open Access

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2nd International Congress on Bacteriology & Infectious Diseases
November 17-19, 2014 DoubleTree by Hilton Hotel Chicago-North Shore, USA

X Sun, Wang Y, Y Yan, H Kim, D Schmidt, W Nie and S Tzipori
ScientificTracks Abstracts: J Bacteriol Parasitol
DOI: 10.4172/2155-9597.S1.006
Clostridium difficile is the major cause of hospital-acquired infectious diarrhea and colitis in developed countries. The pathogenicity of C. difficile is mainly mediated by the release of two potent large exotoxins, toxin A (TcdA) and toxin B (TcdB), both of which are pathogenic and require neutralization to prevent disease occurrence. We have constructed a novel recombinant fusion protein, designated mTcd138, containing the receptor binding domain of TcdA and the glucosyltransferase and cysteine proteinase domains of TcdB and expressed it in Bacillus megaterium. To ensure mTcd138 is atoxic, two point mutations were made in the glucosyltransferase domain of TcdB, which essentially eliminates the toxicity. Parenteral immunizations of mice with mTcd138 induced highly protective antibodies to both toxins and provided full protection against parenteral toxin challenges with lethal doses of toxins and infection with a hyper-virulent C. difficile strain UK6. Our studies demonstrate the potential of mTcd138 as a vaccine candidate against CDI in humans.
X Sun, is an Assistant Professor in research focusing on Clostridium difficile infection at Tufts University, USA. He received his PhD (magna cum laude) in Natural Sciences from University of Kiel, Germany, and did his postdoctoral training in Molecular Microbiology, Cell Biology & Biochemistry at Brown University, USA. He received Young Scientist Award from Federation of European Microbiological Societies in 2002, and Infectious Diseases Fellows Grant from American Society for Microbiology and the Infectious Diseases Society of America in 2008. His research is supported by NIH and private sectors. He is investigating C. difficile toxinmediated signal transduction, leading to the production of proinflammatory mediators. He is also developing preventive and therapeutic approaches targeting C. diffcile toxins and proinflammatory mediators in Clostridium difficile infection.
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